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Presented By: Arslan(13893) Usman(14254) Daniyal(14681)
Abdullah(14659)
Topic:
Cardiac Deseases And Herbs Use Against Them
Presented to: DR. RABEEA KHAN
RIPHAH INSTITUTE OF PHARMACEUTICAL
SCIENCES
PHARMACOGNOSY
CONTENTS
o Hypertension
o Plants Used in Hypertension
a) Rauwolfia Serpentina
b) Veratrum
o Angina & Arrythmias
o Plants used in Angina & Arrythmias:
a)Crataegus hawthorn
b)Convallaria majalis
Congestive Heart Failure
o Plants used in Congestive Heart Failure:
a) Digitalis.
o Atherosclerosis
o Plants used in Atherosclerosis:
a) Allium sativum.
b) Punica granatum.
Introduction
Cardiovascular disease (CVD) is a class of diseases that
involve the heart or blood vessels. Cardiovascular
disease includes coronary artery diseases (CAD) such
as angina, heart arrhythmia, hypertension,
peripheral and central vascular
disease and myocardial infarction (heart failure).
Hypertension
Hypertension is:
High Blood Pressure, a medical condition in which constricted arterial
blood vessels increase the resistance to blood flow, causing an increase
in blood pressure against vessel walls.
• Simply put, as a common disorder in which blood pressure remains
abnormally high.
• Affects ~50 million people in the US
Types of Hypertension
• Types:
– 1. Primary
• Chronic high blood pressure without a source or associated with any other
disease
• Most common form of hypertension
– 2. Secondary
• Elevation of blood pressure associated with another disease such as kidney
disease
• The organs and tissue in your body
need oxygen to survive.
• Oxygen is bound to your blood and is
delivered( after an exchange of
carbon dioxide for oxygen in your
lungs) to your body by blood vessels.
• When your heart beats, it creates
pressure that pushes blood through
your arteries and veins, also known as
blood vessels and capillaries.
• Blood pressure is the force of blood
pushing against your blood vessel
walls.
• Your blood pressure must be within a
normal range to properly deliver this
oxygen rich blood to your organs and
tissues in order to survive.
• When someone has high blood pressure , this increased force makes the heart
work harder to pump blood to the body.
• The increased force puts a strain on both the heart and the blood vessels.
• If the force of the blood flow is high for some time, eventually the tissue that
makes up the walls of the arteries gets stretched beyond its healthy limit.
• This overstretching of the blood vessels makes them more prone to rupture.
• Damages to the vessels results in the development of Atherosclerosis
( hardening of the arteries).
• Uncontrolled high blood pressure increases your risk of serious health
problems, including heart attack and stroke
Causes
• Genetics-some people are prone to hypertension simply based off
of their genetic makeup
• Family History- your risk for high blood pressure/hypertension
increases if it is in your family history
• Environment
– Inactivity
– Stress
– Obesity
– Alcohol
– High Sodium Diet
– Tobacco Use
– Age
– Menopausal Medications
Further Complications of High Blood Pressure
• Thickening of the heart muscle
• Increased workload of the heart
• May lead to other conditions such as:
– Heart attack
– Stroke
– Renal (Kidney) Failure
– Loss of vision
• Those who have higher sensitivity to salt are at
higher risk of hypertension…
So why salt is bad ?
Signs and Symptoms
• Diagnosed through repeat blood pressure readings
• Primary Hypertension does not have symptoms
other than high blood pressure
• Secondary Hypertension
– Most likely caused by Renal Disorders, symptoms
you will see:
• Decreased urine formation
• Increased sodium and water retention
Plants Used In Hypertension
Rauvolfia serpentina
Common Names:Serpentine wood, chandarbagha and Indian snakeroot.
Botanical Name:Rauvolfia serpentina.
Part used: Dried Root.
Family: Apocynaceae.
Geographical regions:
It is distributed in Central and South America, Africa, India, Sri Lanka, Burma, China and Japan
Chemical Constituents:
Rauvolfia root contains more than 200 alkaloids. The major alkaloids are divided into two groups:
Ajmaline group:
Ajmaline, Ajmalinine and Ajmalicine.
Serpentine group: Serpentine and Serpentinine.
Others include:Reserpine, Rescinnamine and Yohimbine,indobine, and deserpidine.
The roots also contain oleoresins, a sterol, unsaturated alcohols, oleic acid, fumaric acid,
glucose, sucrose, a derivative or oxymethylantheraquinone, a strongly fluorescent substance
and mineral salts
Mechanism of Action:
• Reserpine was one of the first drugs used on a large scale to treat systemic
hypertension. It acts by irreversibly blocking the uptake of biogenic amines
(norepinephrine, dopamine, and serotonin) in the storage vesicles of central and
peripheral adrenergic neurons, thus leaving the catecholamines to be destroyed by
the enzyme monoamine oxidase in the cytoplasm.
• The depletion of catecholamines accounts for reserpine's sympatholytic and
antihypertensive actions.
• Reserpine's effects are long lasting, since recovery of sympathetic function
requires synthesis of new storage vesicles, which takes days to weeks.
• Dose:
The daily oral dose of reserpine should be 0.25 mg or less, and as little as 0.05 mg
if given with a diuretic. Using the whole root, the usual adult dose is 50 to 200
mg/d administered once daily or in 2 divided doses
• Uses:
• The root extract obtained is considered to be the best medicine for high
blood pressure, mental agitation, insomnia and also used as a sedative.
• Extracts of R.serpentina is also helpful in curing other diseases such as
fever, malaria, eye diseases, pneumonia, asthma, headache, skin disease
and spleen disorder.
• The plant extract has anti-prostate cancer activity.
• Used in the treatment of cholera.
• Used to treat liver pain, stomach pain and to expel intestinal worms.
• Extracts of the roots are valued for the treatment of intestinal disorders,
particularly diarrhoea and dysentery and also as anathematic.
Veratrum album
Common Name: white hellebore, European white hellebore or white veratrum.
Botanical Name: Veratrum album.
Part Used: Roots and rhizome.
Family:Melanthiaceae.
Geographical distribution:Canada, Alaska, USA and Asia
Chemical Constituents:
Veratrum contains steroidal alkaloids
Veratralbine 0.03
jervine 0.1%
Barytine.
Protoveratridine 0.005%
Pseudo-jervine 0.1%
Rubijervine 0.005%
Protoveratrine 0.1%.
Mechanism of Action:
• Veratrum alkaloids enhance nerve and muscle excitability by increasing sodium ion
conductivity.
• They act on the posterior wall of the left ventricle and the coronary sinus
baroreceptors, causing reflex hypotension and bradycardia via the vagus nerve
(Bezold-Jarisch reflex).
Dose:
• 3 x dilution may be added to water in the proportion of 30 drops of the tincture to
4 fluid ounces of water, the dose of which, in severe cases, is a teaspoonful every
15 minutes.
• For its earlier uses, the dose of the powder is from 1 to 8 grains, gradually and
cautiously increased, commencing with 1 grain, from 20 to 60 minims. Its use
always requires great care.
• Medicinal Uses:
• In the treatment of hypertension.
• In the form of decoction or ointment, as an external
application to kill lice, and cure the itch, pruritis, scabies
and some other cutaneous affections.
• It has been used for the cure of gout.
• It used to be employed in cholera infantum, cholera
morbus and asiatic cholera in all of which it also checks
the vomiting
ANGINA PECTORIS
By Muhammad Usman Sarwar
14254
Angina Pectoris
• is recurring acute chest pain or discomfort resulting from decreased
blood supply to the heart muscle (myocardial ischemia).
• “Increasing Demand of oxygen but the heart can’t supply”
• Generally due to obstruction or spasm of the coronary arteries.
• The chest pain comes either as a form of pressure or discomfort
when blood flow is reduced, your heart does not get as much
oxygen asit needs.
• This lack of oxygen is what causes the pain and discomfort of
angina.
• If you have coronary heart disease, angina is the way your heart
tells you it needs more oxygen
Types
Angina is consisted of three types:
• Stable
• Unstable
• Variant (Prinzmetal's Angina)
Stable Angina
• Most common type
• when the patient has greater than or equal to 70% stenosis
• Induced by physical activity (increase demand of O2), or emotional
stress.
• And can’t be supplied because of partially occluded coronary artery
caused by atherosclerosis)
• The pain is relieved by rest.
Causes of stable angina
• Atherosclerosis of one or more coronary arteries—
arteries supplying blood to the heart muscles.
• Or thickened heart muscle wall, which would require
more oxygen.
– This increase in muscle size can be due to hypertrophic
cardiomyopathy from a genetic cause, or as a result from the heart
having to pump against higher pressures, as is the case in aortic
stenosis, which is a narrowing of the aortic valve, or hypertension.
These larger, thicker heart muscles require more oxygen, and if the
patients can’t meet increasing demands, they feel pain in the form of
angina.
p
Unstable Angina
Dangerous and requires emergency treatment.
Unstable angina is the rupture of the fibrous cap, leading to the blockage of
the artery by clotted blood.
• Occurs with increasing frequency (progression)
• Patients have pain during exercise or stress as well as
during rest—it never really goes away.
• Can lead to MI.
Vasospastic Angina(prinzmetal's Angina)
• Patients may or may not also have atherosclerosis.
• Ischemia, and resulting chest pain is due to coronary
artery vasospasms, meaning the muscles around the
arteries constrict extremely tightly and reduce blood flow
enough cause ischemia.
• Episodes of vasospastic angina can happen anytime.
• The underlying mechanism causing vasospasms isn’t well
understood, but most likely involves vasoconstrictors like
platelet thromboxane A2.
• Coronary artery is constricted severely that all layers
of the heart wall being supplied are affected,
therefore it’s referred to as transmural ischemia.
Plants used in Angina :
Crataegus Hawthorn
Common Name: Hawthorne, Mayblossom, hedgethorn, maybush, mayflower.
Botanical Name: Crataegus oxyacantha & C.monogyna
Part Used: leaves, flowers and fruits
Family:Rosaceae
Geographical distribution:
England and other European countries such as Albania, Bulgaria, Romania,
Hungary, Macedonia and Poland.
Chemical Constituents:
• Hawthorn contains around 1-2% flavonoids,
• Oligomeric proanthocyanidins (1-3%),
• Saponins,
• Phenolic acids (chlorogenic acid, caffeic acid),
• 2-2-Phenylethyl chromone derivatives (in the flowers, leaves and buds)
• Amine (phenethylamine, metoksyfenetylamin, dopamine, acetylcholine and
tyramine) and triterpenes based on ursolic acid and oleanolic acid.
• Anthocyanin is found in the fruit peel and the fruit contains essential oil, pectin,
vitamin C and other substances.
Mechanism of Action:
• Hawthorn works by increasing stroke volume, where the amount of blood per heart beat is
increased, and lowering blood pressure and pulse rate.
• The primary mechanism involves cyclic AMP (adenosine monophosphate). When stimulated,
receptors on the outsides of muscle cell membrane enable the synthesis of adenylyl cyclase.
• The presence of cAMP activates the calcium channels in the muscle cell membranes. In heart
muscle cells, calcium influx promotes increased heart contractility.
• When epinephrine and norepinephrine bind to membrane receptors, a chain reaction is initiated;
the increased calcium level results in increased ionotropic capacity and negative chronotropic
actions.
• The mechanism of cardiac action for Crataegus species is due to the inhibition of the 3‘, 5‘-cyclic
adenosine monophosphate phosphodiesterase.
• Crataegus constituents act as natural angiotensin converting enzyme (ACE) inhibitors. ACE is an
important enzyme involved with blood pressure regulation and also sodium and electrolyte balance
in tissues. Inhibiting ACE also serves to lower blood pressure and strengthen heart muscle
function.
• Crataegus inhibits ACE, presumably due to its procyanidin oligomers. When this enzyme is
inhibited, angiotensin I is not converted to angiotensin II. As a result, the production of aldosterone
is reduced. Since aldosterone promotes water and sodium retention,in its absence sodium and
water are more easily excreted.
• Medicinal Uses:
• Crataegus has long been used as a heart tonic for both hyper-
and hypotension.
• Crataegus also regulates heart rhythm in patients with heart
failure.
• Crataegus to improve aortic contractility in heart failure.
also be helpful in treating elevated cholesterol levels and
atherosclerosis.
• Dose:160 to 1,800 mg/day standardized extracts in divided
doses over 3 to 24 weeks. 900mg in CCF is also safe
Convallaria Majalis
• Common Name:Lily of the valley
Botanical Name: Convallaria majalis
Part Used:Flowers, leaves and root. The fresh leaves
have the most potency.
Family:Asparagaceae.
• Geographical distribution:
Lily of the valley is native to Europe, but is found
abundantly throughout the Eastern United States,
Northern Asia and in England
• Chemical Constituents:
Roughly 38 different cardiac glycosides have been found in lily of
the valley, some among others: convallatoxin, convallotoxole,
convallarin, convallamarin, convalloside,
convallotoxoloside saponins, flavonoids, asparagin etc. Only two of
these substances act directly on the heart.
• Convallamarin, the active principle, a white crystalline powder,
readily soluble in water and in alcohol, but only slightly in ether,
which acts upon the heart like Digitalin, and has also diuretic action,
and Convallarin, which is crystalline in prisms, soluble in alcohol,
slightly soluble in water and has a purgative action. There are also
present a trace of volatile oil, tannin, salts, etc.
Mechanism of Action:
• Herbalists have considered the roots of the Convallaria plant to be a
treatment for a weak heart, shortness of breath tachycardia and
arrythmia.
• The Convallaria plant transforms convalloside (the basic metabolic
glycoside) into convallatoxin and other cardiac glycosides.
• Convallatoxin affects vasoconstriction and vasodilation, and cardiac
stroke volume, pulse pressure and cAMP activity are all enhanced
by Convallaria.
• It is also a lipoxygenase inhibitor
Dosage:
• Tincture (1:5, 40%), 0.5-1.0 ml.
• Infusion: 1 tsp/cup.
• Dried leaves: 60-200mg TID.
• Short term use best (4-6 weeks).
Medicinal Uses:
• It has similar but milder cardiac effects to Digitalis but without the toxic
buildup.
• Exerts a positive inotropic and negative chronotropic action on the heart
and is specific for congestive heart failure with edema.
• It is most indicated in bradycardic and/or arrhythmic forms of heart
failure.
• Mitral stenosis, mitral regurgitation and corpumonale are especially good
indications for its use.
• In aromatherapy, the essential oil of lily of the valley is used to relieve
depression, imbue gentleness, happiness, modesty, a sweet disposition
and sense of security.
• The herb has been used for weak contractions during childbirth as well as
for epileptic seizures, strokes, angina and ensuing paralysis, conjunctivitis
and leprosy.
Toxicity:
Signs of toxicity: nausea, vomiting, violent purging, cardiac arrhythmias,
increased blood pressure, restlessness, trembling, mental confusion,
extreme weakness, depression, collapse of circulation, and death. Monitor
BP and edema. Berries are poisonous.
CONGESTIVE HEART FAILURE
By Abdulllah Tariq
14659
CONGESTIVE CARDIAC FAILURE
• Definition:
Heart failure in which the heart is unable to maintain
adequate circulation of blood in the tissues of the body
or increase in myocardial oxygen demand and decreased
myocardial oxygen supply.
OR
It is a common clinical disorder that results in
pulmonary vascular. congestion and reduced cardiac
output. CHF patient usually presents with dyspnea and
respiratory failure.
PATHOPHYSIOLOGY
Pathology:
• CHF arises as a consequence of an abnormality in
cardiac structure, function, rhythm, or conduction.
• Ventricular dysfunction accounts for the majority of
cases and results mainly from myocardial infarction
(systolic dysfunction), hypertension (diastolic and
systolic dysfunction), or in many cases both.
• Degenerative valve disease, idiopathic
cardiomyopathy, and alcoholic cardiomyopathy are
also major causes of CHF.
CHF indicates inability of the heart to maintain
adequate oxygen delivery; it is also a systemic response
attempting to compensate for the inadequacy. The
determinants of cardiac output include heart rate and
stroke volume(the volume of blood pumped from the left
ventricle per beat.). The stroke volume is further
determined by the preload (the volume that enters the
left ventricle),contractility and afterload (the impedance
of the flow from the left ventricle).
PATHOPHYSIOLOGY Cont..
There are 2 mechanisms of reduced cardiac
output and heart failure:
• Systolic dysfunction
• Diastolic dysfunction
Systolic Dysfunction
• The most common causes of systolic dysfunction
(defined by a left-ventricular ejection fraction of
50%) are ischemic heart disease, idiopathic dilated
cardiomyopathy, hypertension, and valvular heart
disease.
Diastolic Dysfunction
• Diastolic dysfunction (defined as dysfunction of left-
ventricular filling with preserved systolic function)
may occur in up to 40–50% of patients with heart
failure and it increases in frequency with each
decade of life.
• Causes: Hypertension, ischemic heart disease,
hypertrophic cardiomyopathy, and restrictive
cardiomyopathy.
PATHOPHYSIOLOGY
Physiology:
• Cardiac structural abnormality; ardiovascular
response to poor perfusion with the activation of the
neurohumoral system.
• Activation of the renin-angiotensin system attempts
to increase preload by stimulating retention of salt
and water, increasing vasoconstriction, and
augmenting cardiac contractility. Initially, this
response will suffice, but prolonged activation results
in loss of myocytes and maladaptive changes in the
surviving myocytes.
• The stressed myocardium undergoes remodeling and
dilation in response to the insult.
Cont…
• This process also has detrimental effects on the
functioning of the lungs, kidneys, muscles, blood
vessels, and probably other organs.
• Remodeling also results in additional cardiac
decompensation from complications, including mitral
regurgitation and cardiac arrhythmias from atrial
remodeling.
Diagnosis and Treatment
Diagnosis:
• The measurement of serum natriuretic
peptide and echocardiography have
substantially improved the accuracy of
diagnosis.
• Physical examination,chest radiography
• Pulmonary congestion (with crackles and wheezing)
is predominant.
Treatment
Plants used in Congestive Heart Failure:
DIGITALIS LEAVES
• Common Name: Fox glove and purple foxglove.
Botanical Name:Digitalis purpurea Linn
Part Used: Dried Leaves.
• Family:Scrophulariaceae.
• Geographical distribution: It is mainly found in
England, Germany, France, North
• America, India, Iraq, Japan, Kurdistan, Mexico, Nepal.
Chemical Constituents:
Digitalis essentially contains three important primary glycosides namely:
• Purpurea glycoside A, Purpurea glycoside B, and Purpurea glycoside C,
which upon hydrolysis give rise to digitoxin, gitoxin and gitalin/gitaloxin
respectively.
• These secondary glcosides on further hydrolysis yields noncarbohydrate
moieties (called aglycones or genins) digitoxigenin, gitoxigenin and
gitaligenin or gitaloxigenin respectively.
• The crude drug also contains a good number of other glycosides (e.g.;
digitalin, diginin)
• Saponins (e.g.; digitonin, gitin and digitosaponin)
• Tannins, gallic, formic, acetic, succinic and benzoic acids, fatty acids and
• Enzyme digipuridase solely responsible for hydrolysis of purpurea
glycosides.
Mechanism of action
• Digitalis works by inhibiting sodium-potassium ATPase. This results
in an increased intracellular concentration of sodium ions and thus
a decreased concentration gradient across the cell membrane. This
increase in intracellular sodium causes the Na/Ca exchanger to
reverse potential, i.e., transition from pumping sodium into the cell
in exchange for pumping calcium out of the cell, to pumping sodium
out of the cell in exchange for pumping calcium into the cell. This
leads to an increase in cytoplasmic calcium concentration, which
improves cardiac contractility.
• As a result of increased contractility, stroke volume is increased.
Ultimately, digitalis increases cardiac output (Cardiac Output=Stroke
Volume x Heart Rate). This is the mechanism that makes this drug a
popular treatment for congestive heart failure, which is
characterized by low cardiac output. Digitalis also has a vagal effect
on the parasympathetic nervous system, and as such is used in re-
entrant cardiac arrhythmias and to slow the ventricular rate
during atrial fibrillation.
Medicinal Uses:
• Digitalis enhances the force of contraction of heart muscle which
ultimately affords an increased cardiac output, decreased size of heart,
decreased venous pressure and above all the decreased blood volume.
• Thus digitalis together with its various marketed preparations are
employed profusely as vital cardiotonics in the management and control
of different kinds of congestive heart failure, atrial flutter, atrial fibrillation,
supraventricular tachycardia and premature extra systoles.
Dosage:
Administer one-half the total loading dose initially (all formulations), then
give one-fourth the total loading dose every 6 to 8 hours for two doses (IV
and tablets), or give additional fractions every 4 to 8 hours (oral solution).
-IV: 8 to 12 mcg/kg
-Tablets: 10 to 15 mcg/kg
-Oral solution: 10 to 15 mcg/kg.
ATHEROSCLEROSIS
By: Daniyal Khan
14681
Intro to Atherosclerosis
• Atherosclerosis (also known as Arteriosclerotic
Vascular Disease or ASVD) the condition in which an
artery wall thickens as the result of a build-up of fatty
materials such as cholesterol affecting arterial blood
vessels, a chronic inflammatory response in the walls
of arteries due to the accumulation of macrophage
white blood cells and promoted by Low-density
lipoproteins without adequate removal of fats and
cholesterol from the macrophages by functional high
density lipoproteins
• It is commonly referred to as a hardening or furring of
the arteries.
• It is caused by the formation of multiple plaqueswithin
the arteries.
• It can restrict blood flow. These plaques can also burst,
causing a blood clot.
• Although atherosclerosis is often considered a heart
problem, it can affect arteries anywhere in your body.
• Atherosclerosis is a preventable and treatable condition.
Causes
Atherosclerosis starts with damage or injury to the
inner layer of an artery. The damage may be caused
by:
• High blood pressure
• High cholesterol
• An irritant, such as nicotine
• Certain diseases, such as diabetes
Pathophysiology
• Atherosclerosis develops as a chronic inflammatory
response of the arterial wall to endothelial injury.
• Lesion progression occurs through interactions of
modified lipoproteins, monocyte-derived macrophages,
T-lymphocytes, and the normal cellular constituent of
the arterial wall.
• The contemporary view of atherosclerosis is expressed
by the response-to-injury hypothesis.
Response-to-injury hypothesis
• The following are the
steps involved in the
hypothesis:
1. Chronic endothelial
injury
2. Accumulation of
lipoproteins
3. Monocyte adhesion to
the endothelium
4. SMC proliferations and
ECM production
5. factor release
6. platelet adhesion
1. Chronic endothelial injury
• with resultant endothelial dysfunction, causing
increased permeability, leukocyte adhesion, and
thrombosis
Response-to-injury hypothesis
2. Accumulation of lipoproteins
• (mainly LDL and its oxidized forms) in the vessel wall.
Low-density lipoprotein molecules (LDL) becoming
oxidized (ldl-ox) by free radicals, particularly oxygen
free (ROS). When oxidized LDL comes in contact with
an artery wall, a series of reactions occur to repair the
damage to the artery wall caused by oxidized LDL.
Cholesterol can move in the bloodstream only by being
transported by lipoproteins
Response-to-injury hypothesis
3. Monocyte adhesion to the endothelium
• followed by migration into the intima and
transformation into macrophages and foam cells. The
body's immune system responds to the damage to the
artery wall caused by oxidized LDL by sending
specialized white blood cells (macrophages and T-
lymphocytes) to absorb the oxidized-LDL forming
specialized foam cells. Unfortunately, these white
blood cells are not able to process the oxidized-LDL,
and ultimately grow then rupture, depositing a greater
amount of oxidized cholesterol into the artery wall.
This triggers more white blood cells, continuing the
cycle.
Response-to-injury hypothesis
4. platelet adhesion
5. factor release
• from activated platelet,
macrophages and vascular wall
cells, inducing SMC recruitment,
either from the media or from the
circulating precursors
Response-to-injury hypothesis
6. SMC proliferations and ECM production.
• Eventually, the artery becomes
inflamed. The cholesterol plaque causes
the smooth muscle cells to enlarge and
form a hard cover over the affected
area. This hard cover is what causes a
narrowing of the artery, reduces the
blood flow and increases blood
pressure.
Response-to-injury hypothesis
7. Lipid accumulation
• both extracellularly and within cells
(macrophages and SMC’s). accumulation if
lipid-containing macrophages in the intima
gives rise to “fatty streaks”, with further
evolution, a fibrofatty atheroma consisting of
proliferated SMC, foam cells, extracellular
lipid, and ECM is formed.
Response-to-injury hypothesis
Atherosclerosis symptoms depend on which arteries are
affected. For example:
• Atherosclerosis in heart arteries, have symptoms similar to
those of a heart attack, such as chest pain (angina).
• Atherosclerosis in the arteries leading to brain, have
symptoms such as sudden numbness or weakness in your
arms or legs, difficulty speaking or slurred speech, or
drooping muscles in your face.
• Atherosclerosis in the arteries in arms and legs, produces
decreased blood flow is called peripheral artery occlusive
disease (PAOD).have symptoms such as leg pain when
walking
• Sometimes atherosclerosis causes erectile dysfunction in
men.
Symptoms
Depending on the results of the physical exam, doctors may
suggest one or more diagnostic tests, including:
• Blood tests.
• Doppler ultrasound
• Ankle-brachial index.
• Other imaging tests.
• Angiogram.
• Electrocardiogram (ECG).
Tests and diagnosis
Plants used in Atherosclerosis
Allium sativum
• Common Name:Garlic.
Botanical Name:Allium sativum.
• Part Used:Bulbs and Rhizome.
Family: Amaryllidaceae.
Geographical distribution:Garlic is native to Central Asia (Kazakhstan,
Kyrgyzstan, Turkmenistan, Tadzhikistan and Uzbekistan) and northeastern
Iran
• Chemical costituents:
Garlic contains 0.1-0.36% of a volatile oil. These are generally considered to
be responsible for most of the pharmacological properties of garlic. Garlic
contains at least 33 sulfur compounds like aliin, allicin, ajoene, allylpropl,
diallyl, trisulfide, sallylcysteine, vinyldithiines, S-allylmercaptocystein, and
others. Besides sulfure compounds garlic contains 17 amino acids and their
glycosides, arginine and others.
Minerals such as selenium and enzymes like allinase, peroxidases,
myrosinase etc.
the most biologically active compounds, allicin (diallylthiousulfinate or
diallyl disulfide) does not exist in garlic until it is crushed or cut; injury to the
garlic bulb activates the enzyme allinase, which metabolizes alliin to allicin
• Mechanism of Action:
• Intact cells of garlic bulbs include an odorless, sulfur-containing amino
acid known as allinin.
• When garlic is crushed, allinin comes into contact with allinase, which
converts allinin to allicin. Allicin has potent antibacterial properties, but it
is also highly odoriferous and unstable.
• Ajoenes, self-condensation products of allicin, appear to be responsible
for garlic's antithrombotic activity.
• Fresh garlic releases allicin in the mouth during the chewing process. Dried
garlic preparations lack allicin but contain allinin and allinase. Since
allinase is inactivated in the stomach, dried garlic preparations should be
coated with enteric so that they pass through the stomach into the small
intestine where allinin can be enzymatically converted to allicin.
• Medicinal Uses:
• Lipid-lowering Effects: Garlic's lipid lowering effects may occur via inhibition of
HMG-CoA reductase or other enzymes, possibly by diallyl di- and trisulphide
components of garlic.
• Platelet Effects: Garlic and its derived compound ajoene have demonstrated
inhibition of platelet aggregation In vitro and in animals, and reduction of
platelet-dependent thrombus formation.
• Fibrinolytic Effects: Increased fibrinolytic activity may account for some degree of
garlic's anti-clotting effects, involving fibrinogen and plasminogen.
• Antimicrobial Effects (Bacteria, Fungi, Yeast): Garlic has been demonstrated In
vitro to exert activity against multiple pathogens, including bacteria, including
resistant strains, mycobacteria, Helicobacter pylori and fungi. Garlic extract has
been found to be bactericidal to Histoplasmacapsulatum.Ajoene alone possesses
antibacterial activity against both gram positive and negative bacterial species
and inhibits yeast growth In vitro, and the disulfide bond in ajoene may be
responsible for these effects.
• Lowering of blood glucose and blood pressure; and liver protection.
• Unani physicians also use garlic to treat paralysis, forgetfulness, tremor, colic
pains, internal ulcers and fevers.
• DOSAGE:
1. Atherosclerosis:A 300 mg garlic powder tablet taken as a
single dose or three times daily.
• 2. For colon cancer and rectal cancer: Capsules containing 2.4
mL of aged garlic extract taken daily for 12 months have been
used.
• 3. For high blood pressure: 300 mg to 1500 mg of garlic
tablets taken in divided doses daily for 24 weeks.
• 4. For fungal skin infections (ringworm, jock itch, athlete's
foot): garlic ingredient ajoene as a 0.4% cream, 0.6% gel, and
1% gel applied twice daily for one week has been used.
Punica granatum
• Common Name:Pomegranate.
Botanical Name: Punicagranatum Linn
• Part Used: Fruit
• Family: Lythraceae
• Geographical region:
Pomegranate is native to a region from Iran to northern India. Pomegranates have
been cultivated throughout the Middle East, South Asia, and Mediterranean
region for several millennia, and also thrive in the drier climates of California and
Arizona
• Chemical constituents:
• Punicalagin
• Punicallin
• Punic acid
• Gallagicacid
• Granatin A
• Casuarinin,
• Pseudopelletierene
• Mechanism of action and medicinal uses:
• The potential therapeutic properties of pomegranate are wide-ranging and include treatment and
prevention of cancer, cardiovascular disease, diabetes, dental conditions, erectile dysfunction, and
protection from ultraviolet (UV) radiation.
• Other potential applications include infant brain ischemia, Alzheimer’s disease, male infertility,
arthritis, and obesity.
Plant pacifies tridosha, tapeworm infestation,
• Increase digestive power; alleviate fatigue and thirst and aphrodisiac.
• The juice of fresh leaves and young Pomegranate is given in dysentery.
• The powdered bark is given for expelling roundworms.
• According to Kirtikar and Basu (1935) the unripe fruits and flowers are useful in inducing vomiting,
the rind of the fruit is given in diarrhoea and dysentery.
• They also strengthen the gums.
• Ripe fruit is tonic, laxative and enriches the blood.
• The flower-buds are astringent, and are given in chronic diarrhoea and dysentery.
• Dose:
• As an antioxidant 1000 milligrams of pomegranate
extract in the form of POMx™ capsules has been
taken by mouth daily for four weeks.
A dose of 50 milliliters of pomegranate juice has
been taken by mouth daily for three months.
• A dose of 100 grams of fresh pomegranate fruit has
been taken by mouth for 10 days.
REFERENCES
• http://jamanetwork.com/journals/jamainternalmedicine/fulla
rticle/210378
• http://www.sigmaaldrich.com/life-science/nutrition-
research/learning-center/plant-profiler/allium-sativum.html
• Bentley and Trimen, Med. Plants 281. 3. Benkeblia, N. 2004.
Antimicrobial activity of essential oil extracts of various onions
Allium cepa& Garlic (Alliceasatium) lebeusmwiss-uTechnol.
373.
• Chemical constituents of cultivated onion Allium
cepaLiliaceae.
• https://restorativemedicine.org/journal/the-use-of-
convallaria-and-crataegus-in-the-treatment-of-cardiac-
dysfunction/.
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Cardiac Deseases And Herbs Use Against Them

  • 1. Presented By: Arslan(13893) Usman(14254) Daniyal(14681) Abdullah(14659) Topic: Cardiac Deseases And Herbs Use Against Them Presented to: DR. RABEEA KHAN RIPHAH INSTITUTE OF PHARMACEUTICAL SCIENCES PHARMACOGNOSY
  • 2. CONTENTS o Hypertension o Plants Used in Hypertension a) Rauwolfia Serpentina b) Veratrum o Angina & Arrythmias o Plants used in Angina & Arrythmias: a)Crataegus hawthorn b)Convallaria majalis Congestive Heart Failure o Plants used in Congestive Heart Failure: a) Digitalis. o Atherosclerosis o Plants used in Atherosclerosis: a) Allium sativum. b) Punica granatum.
  • 3. Introduction Cardiovascular disease (CVD) is a class of diseases that involve the heart or blood vessels. Cardiovascular disease includes coronary artery diseases (CAD) such as angina, heart arrhythmia, hypertension, peripheral and central vascular disease and myocardial infarction (heart failure).
  • 5. Hypertension is: High Blood Pressure, a medical condition in which constricted arterial blood vessels increase the resistance to blood flow, causing an increase in blood pressure against vessel walls. • Simply put, as a common disorder in which blood pressure remains abnormally high. • Affects ~50 million people in the US Types of Hypertension • Types: – 1. Primary • Chronic high blood pressure without a source or associated with any other disease • Most common form of hypertension – 2. Secondary • Elevation of blood pressure associated with another disease such as kidney disease
  • 6. • The organs and tissue in your body need oxygen to survive. • Oxygen is bound to your blood and is delivered( after an exchange of carbon dioxide for oxygen in your lungs) to your body by blood vessels. • When your heart beats, it creates pressure that pushes blood through your arteries and veins, also known as blood vessels and capillaries. • Blood pressure is the force of blood pushing against your blood vessel walls. • Your blood pressure must be within a normal range to properly deliver this oxygen rich blood to your organs and tissues in order to survive.
  • 7. • When someone has high blood pressure , this increased force makes the heart work harder to pump blood to the body. • The increased force puts a strain on both the heart and the blood vessels. • If the force of the blood flow is high for some time, eventually the tissue that makes up the walls of the arteries gets stretched beyond its healthy limit. • This overstretching of the blood vessels makes them more prone to rupture. • Damages to the vessels results in the development of Atherosclerosis ( hardening of the arteries). • Uncontrolled high blood pressure increases your risk of serious health problems, including heart attack and stroke
  • 8. Causes • Genetics-some people are prone to hypertension simply based off of their genetic makeup • Family History- your risk for high blood pressure/hypertension increases if it is in your family history • Environment – Inactivity – Stress – Obesity – Alcohol – High Sodium Diet – Tobacco Use – Age – Menopausal Medications
  • 9. Further Complications of High Blood Pressure • Thickening of the heart muscle • Increased workload of the heart • May lead to other conditions such as: – Heart attack – Stroke – Renal (Kidney) Failure – Loss of vision
  • 10. • Those who have higher sensitivity to salt are at higher risk of hypertension… So why salt is bad ?
  • 11. Signs and Symptoms • Diagnosed through repeat blood pressure readings • Primary Hypertension does not have symptoms other than high blood pressure • Secondary Hypertension – Most likely caused by Renal Disorders, symptoms you will see: • Decreased urine formation • Increased sodium and water retention
  • 12. Plants Used In Hypertension
  • 13. Rauvolfia serpentina Common Names:Serpentine wood, chandarbagha and Indian snakeroot. Botanical Name:Rauvolfia serpentina. Part used: Dried Root. Family: Apocynaceae. Geographical regions: It is distributed in Central and South America, Africa, India, Sri Lanka, Burma, China and Japan Chemical Constituents: Rauvolfia root contains more than 200 alkaloids. The major alkaloids are divided into two groups: Ajmaline group: Ajmaline, Ajmalinine and Ajmalicine. Serpentine group: Serpentine and Serpentinine. Others include:Reserpine, Rescinnamine and Yohimbine,indobine, and deserpidine. The roots also contain oleoresins, a sterol, unsaturated alcohols, oleic acid, fumaric acid, glucose, sucrose, a derivative or oxymethylantheraquinone, a strongly fluorescent substance and mineral salts
  • 14. Mechanism of Action: • Reserpine was one of the first drugs used on a large scale to treat systemic hypertension. It acts by irreversibly blocking the uptake of biogenic amines (norepinephrine, dopamine, and serotonin) in the storage vesicles of central and peripheral adrenergic neurons, thus leaving the catecholamines to be destroyed by the enzyme monoamine oxidase in the cytoplasm. • The depletion of catecholamines accounts for reserpine's sympatholytic and antihypertensive actions. • Reserpine's effects are long lasting, since recovery of sympathetic function requires synthesis of new storage vesicles, which takes days to weeks. • Dose: The daily oral dose of reserpine should be 0.25 mg or less, and as little as 0.05 mg if given with a diuretic. Using the whole root, the usual adult dose is 50 to 200 mg/d administered once daily or in 2 divided doses
  • 15. • Uses: • The root extract obtained is considered to be the best medicine for high blood pressure, mental agitation, insomnia and also used as a sedative. • Extracts of R.serpentina is also helpful in curing other diseases such as fever, malaria, eye diseases, pneumonia, asthma, headache, skin disease and spleen disorder. • The plant extract has anti-prostate cancer activity. • Used in the treatment of cholera. • Used to treat liver pain, stomach pain and to expel intestinal worms. • Extracts of the roots are valued for the treatment of intestinal disorders, particularly diarrhoea and dysentery and also as anathematic.
  • 16. Veratrum album Common Name: white hellebore, European white hellebore or white veratrum. Botanical Name: Veratrum album. Part Used: Roots and rhizome. Family:Melanthiaceae. Geographical distribution:Canada, Alaska, USA and Asia Chemical Constituents: Veratrum contains steroidal alkaloids Veratralbine 0.03 jervine 0.1% Barytine. Protoveratridine 0.005% Pseudo-jervine 0.1% Rubijervine 0.005% Protoveratrine 0.1%.
  • 17. Mechanism of Action: • Veratrum alkaloids enhance nerve and muscle excitability by increasing sodium ion conductivity. • They act on the posterior wall of the left ventricle and the coronary sinus baroreceptors, causing reflex hypotension and bradycardia via the vagus nerve (Bezold-Jarisch reflex). Dose: • 3 x dilution may be added to water in the proportion of 30 drops of the tincture to 4 fluid ounces of water, the dose of which, in severe cases, is a teaspoonful every 15 minutes. • For its earlier uses, the dose of the powder is from 1 to 8 grains, gradually and cautiously increased, commencing with 1 grain, from 20 to 60 minims. Its use always requires great care.
  • 18. • Medicinal Uses: • In the treatment of hypertension. • In the form of decoction or ointment, as an external application to kill lice, and cure the itch, pruritis, scabies and some other cutaneous affections. • It has been used for the cure of gout. • It used to be employed in cholera infantum, cholera morbus and asiatic cholera in all of which it also checks the vomiting
  • 19. ANGINA PECTORIS By Muhammad Usman Sarwar 14254
  • 20. Angina Pectoris • is recurring acute chest pain or discomfort resulting from decreased blood supply to the heart muscle (myocardial ischemia). • “Increasing Demand of oxygen but the heart can’t supply” • Generally due to obstruction or spasm of the coronary arteries. • The chest pain comes either as a form of pressure or discomfort when blood flow is reduced, your heart does not get as much oxygen asit needs. • This lack of oxygen is what causes the pain and discomfort of angina. • If you have coronary heart disease, angina is the way your heart tells you it needs more oxygen
  • 21. Types Angina is consisted of three types: • Stable • Unstable • Variant (Prinzmetal's Angina)
  • 22. Stable Angina • Most common type • when the patient has greater than or equal to 70% stenosis • Induced by physical activity (increase demand of O2), or emotional stress. • And can’t be supplied because of partially occluded coronary artery caused by atherosclerosis) • The pain is relieved by rest.
  • 23. Causes of stable angina • Atherosclerosis of one or more coronary arteries— arteries supplying blood to the heart muscles. • Or thickened heart muscle wall, which would require more oxygen. – This increase in muscle size can be due to hypertrophic cardiomyopathy from a genetic cause, or as a result from the heart having to pump against higher pressures, as is the case in aortic stenosis, which is a narrowing of the aortic valve, or hypertension. These larger, thicker heart muscles require more oxygen, and if the patients can’t meet increasing demands, they feel pain in the form of angina.
  • 24. p
  • 25. Unstable Angina Dangerous and requires emergency treatment. Unstable angina is the rupture of the fibrous cap, leading to the blockage of the artery by clotted blood. • Occurs with increasing frequency (progression) • Patients have pain during exercise or stress as well as during rest—it never really goes away. • Can lead to MI.
  • 26.
  • 27. Vasospastic Angina(prinzmetal's Angina) • Patients may or may not also have atherosclerosis. • Ischemia, and resulting chest pain is due to coronary artery vasospasms, meaning the muscles around the arteries constrict extremely tightly and reduce blood flow enough cause ischemia. • Episodes of vasospastic angina can happen anytime. • The underlying mechanism causing vasospasms isn’t well understood, but most likely involves vasoconstrictors like platelet thromboxane A2.
  • 28. • Coronary artery is constricted severely that all layers of the heart wall being supplied are affected, therefore it’s referred to as transmural ischemia.
  • 29.
  • 30. Plants used in Angina :
  • 31. Crataegus Hawthorn Common Name: Hawthorne, Mayblossom, hedgethorn, maybush, mayflower. Botanical Name: Crataegus oxyacantha & C.monogyna Part Used: leaves, flowers and fruits Family:Rosaceae Geographical distribution: England and other European countries such as Albania, Bulgaria, Romania, Hungary, Macedonia and Poland. Chemical Constituents: • Hawthorn contains around 1-2% flavonoids, • Oligomeric proanthocyanidins (1-3%), • Saponins, • Phenolic acids (chlorogenic acid, caffeic acid), • 2-2-Phenylethyl chromone derivatives (in the flowers, leaves and buds) • Amine (phenethylamine, metoksyfenetylamin, dopamine, acetylcholine and tyramine) and triterpenes based on ursolic acid and oleanolic acid. • Anthocyanin is found in the fruit peel and the fruit contains essential oil, pectin, vitamin C and other substances.
  • 32. Mechanism of Action: • Hawthorn works by increasing stroke volume, where the amount of blood per heart beat is increased, and lowering blood pressure and pulse rate. • The primary mechanism involves cyclic AMP (adenosine monophosphate). When stimulated, receptors on the outsides of muscle cell membrane enable the synthesis of adenylyl cyclase. • The presence of cAMP activates the calcium channels in the muscle cell membranes. In heart muscle cells, calcium influx promotes increased heart contractility. • When epinephrine and norepinephrine bind to membrane receptors, a chain reaction is initiated; the increased calcium level results in increased ionotropic capacity and negative chronotropic actions. • The mechanism of cardiac action for Crataegus species is due to the inhibition of the 3‘, 5‘-cyclic adenosine monophosphate phosphodiesterase. • Crataegus constituents act as natural angiotensin converting enzyme (ACE) inhibitors. ACE is an important enzyme involved with blood pressure regulation and also sodium and electrolyte balance in tissues. Inhibiting ACE also serves to lower blood pressure and strengthen heart muscle function. • Crataegus inhibits ACE, presumably due to its procyanidin oligomers. When this enzyme is inhibited, angiotensin I is not converted to angiotensin II. As a result, the production of aldosterone is reduced. Since aldosterone promotes water and sodium retention,in its absence sodium and water are more easily excreted.
  • 33. • Medicinal Uses: • Crataegus has long been used as a heart tonic for both hyper- and hypotension. • Crataegus also regulates heart rhythm in patients with heart failure. • Crataegus to improve aortic contractility in heart failure. also be helpful in treating elevated cholesterol levels and atherosclerosis. • Dose:160 to 1,800 mg/day standardized extracts in divided doses over 3 to 24 weeks. 900mg in CCF is also safe
  • 34. Convallaria Majalis • Common Name:Lily of the valley Botanical Name: Convallaria majalis Part Used:Flowers, leaves and root. The fresh leaves have the most potency. Family:Asparagaceae. • Geographical distribution: Lily of the valley is native to Europe, but is found abundantly throughout the Eastern United States, Northern Asia and in England
  • 35. • Chemical Constituents: Roughly 38 different cardiac glycosides have been found in lily of the valley, some among others: convallatoxin, convallotoxole, convallarin, convallamarin, convalloside, convallotoxoloside saponins, flavonoids, asparagin etc. Only two of these substances act directly on the heart. • Convallamarin, the active principle, a white crystalline powder, readily soluble in water and in alcohol, but only slightly in ether, which acts upon the heart like Digitalin, and has also diuretic action, and Convallarin, which is crystalline in prisms, soluble in alcohol, slightly soluble in water and has a purgative action. There are also present a trace of volatile oil, tannin, salts, etc.
  • 36. Mechanism of Action: • Herbalists have considered the roots of the Convallaria plant to be a treatment for a weak heart, shortness of breath tachycardia and arrythmia. • The Convallaria plant transforms convalloside (the basic metabolic glycoside) into convallatoxin and other cardiac glycosides. • Convallatoxin affects vasoconstriction and vasodilation, and cardiac stroke volume, pulse pressure and cAMP activity are all enhanced by Convallaria. • It is also a lipoxygenase inhibitor Dosage: • Tincture (1:5, 40%), 0.5-1.0 ml. • Infusion: 1 tsp/cup. • Dried leaves: 60-200mg TID. • Short term use best (4-6 weeks).
  • 37. Medicinal Uses: • It has similar but milder cardiac effects to Digitalis but without the toxic buildup. • Exerts a positive inotropic and negative chronotropic action on the heart and is specific for congestive heart failure with edema. • It is most indicated in bradycardic and/or arrhythmic forms of heart failure. • Mitral stenosis, mitral regurgitation and corpumonale are especially good indications for its use. • In aromatherapy, the essential oil of lily of the valley is used to relieve depression, imbue gentleness, happiness, modesty, a sweet disposition and sense of security. • The herb has been used for weak contractions during childbirth as well as for epileptic seizures, strokes, angina and ensuing paralysis, conjunctivitis and leprosy. Toxicity: Signs of toxicity: nausea, vomiting, violent purging, cardiac arrhythmias, increased blood pressure, restlessness, trembling, mental confusion, extreme weakness, depression, collapse of circulation, and death. Monitor BP and edema. Berries are poisonous.
  • 38. CONGESTIVE HEART FAILURE By Abdulllah Tariq 14659
  • 39. CONGESTIVE CARDIAC FAILURE • Definition: Heart failure in which the heart is unable to maintain adequate circulation of blood in the tissues of the body or increase in myocardial oxygen demand and decreased myocardial oxygen supply. OR It is a common clinical disorder that results in pulmonary vascular. congestion and reduced cardiac output. CHF patient usually presents with dyspnea and respiratory failure.
  • 40. PATHOPHYSIOLOGY Pathology: • CHF arises as a consequence of an abnormality in cardiac structure, function, rhythm, or conduction. • Ventricular dysfunction accounts for the majority of cases and results mainly from myocardial infarction (systolic dysfunction), hypertension (diastolic and systolic dysfunction), or in many cases both. • Degenerative valve disease, idiopathic cardiomyopathy, and alcoholic cardiomyopathy are also major causes of CHF.
  • 41. CHF indicates inability of the heart to maintain adequate oxygen delivery; it is also a systemic response attempting to compensate for the inadequacy. The determinants of cardiac output include heart rate and stroke volume(the volume of blood pumped from the left ventricle per beat.). The stroke volume is further determined by the preload (the volume that enters the left ventricle),contractility and afterload (the impedance of the flow from the left ventricle).
  • 42. PATHOPHYSIOLOGY Cont.. There are 2 mechanisms of reduced cardiac output and heart failure: • Systolic dysfunction • Diastolic dysfunction
  • 43. Systolic Dysfunction • The most common causes of systolic dysfunction (defined by a left-ventricular ejection fraction of 50%) are ischemic heart disease, idiopathic dilated cardiomyopathy, hypertension, and valvular heart disease.
  • 44. Diastolic Dysfunction • Diastolic dysfunction (defined as dysfunction of left- ventricular filling with preserved systolic function) may occur in up to 40–50% of patients with heart failure and it increases in frequency with each decade of life. • Causes: Hypertension, ischemic heart disease, hypertrophic cardiomyopathy, and restrictive cardiomyopathy.
  • 45. PATHOPHYSIOLOGY Physiology: • Cardiac structural abnormality; ardiovascular response to poor perfusion with the activation of the neurohumoral system. • Activation of the renin-angiotensin system attempts to increase preload by stimulating retention of salt and water, increasing vasoconstriction, and augmenting cardiac contractility. Initially, this response will suffice, but prolonged activation results in loss of myocytes and maladaptive changes in the surviving myocytes. • The stressed myocardium undergoes remodeling and dilation in response to the insult.
  • 46. Cont… • This process also has detrimental effects on the functioning of the lungs, kidneys, muscles, blood vessels, and probably other organs. • Remodeling also results in additional cardiac decompensation from complications, including mitral regurgitation and cardiac arrhythmias from atrial remodeling.
  • 47. Diagnosis and Treatment Diagnosis: • The measurement of serum natriuretic peptide and echocardiography have substantially improved the accuracy of diagnosis. • Physical examination,chest radiography • Pulmonary congestion (with crackles and wheezing) is predominant.
  • 49. Plants used in Congestive Heart Failure:
  • 50. DIGITALIS LEAVES • Common Name: Fox glove and purple foxglove. Botanical Name:Digitalis purpurea Linn Part Used: Dried Leaves. • Family:Scrophulariaceae. • Geographical distribution: It is mainly found in England, Germany, France, North • America, India, Iraq, Japan, Kurdistan, Mexico, Nepal.
  • 51. Chemical Constituents: Digitalis essentially contains three important primary glycosides namely: • Purpurea glycoside A, Purpurea glycoside B, and Purpurea glycoside C, which upon hydrolysis give rise to digitoxin, gitoxin and gitalin/gitaloxin respectively. • These secondary glcosides on further hydrolysis yields noncarbohydrate moieties (called aglycones or genins) digitoxigenin, gitoxigenin and gitaligenin or gitaloxigenin respectively. • The crude drug also contains a good number of other glycosides (e.g.; digitalin, diginin) • Saponins (e.g.; digitonin, gitin and digitosaponin) • Tannins, gallic, formic, acetic, succinic and benzoic acids, fatty acids and • Enzyme digipuridase solely responsible for hydrolysis of purpurea glycosides.
  • 52. Mechanism of action • Digitalis works by inhibiting sodium-potassium ATPase. This results in an increased intracellular concentration of sodium ions and thus a decreased concentration gradient across the cell membrane. This increase in intracellular sodium causes the Na/Ca exchanger to reverse potential, i.e., transition from pumping sodium into the cell in exchange for pumping calcium out of the cell, to pumping sodium out of the cell in exchange for pumping calcium into the cell. This leads to an increase in cytoplasmic calcium concentration, which improves cardiac contractility. • As a result of increased contractility, stroke volume is increased. Ultimately, digitalis increases cardiac output (Cardiac Output=Stroke Volume x Heart Rate). This is the mechanism that makes this drug a popular treatment for congestive heart failure, which is characterized by low cardiac output. Digitalis also has a vagal effect on the parasympathetic nervous system, and as such is used in re- entrant cardiac arrhythmias and to slow the ventricular rate during atrial fibrillation.
  • 53. Medicinal Uses: • Digitalis enhances the force of contraction of heart muscle which ultimately affords an increased cardiac output, decreased size of heart, decreased venous pressure and above all the decreased blood volume. • Thus digitalis together with its various marketed preparations are employed profusely as vital cardiotonics in the management and control of different kinds of congestive heart failure, atrial flutter, atrial fibrillation, supraventricular tachycardia and premature extra systoles. Dosage: Administer one-half the total loading dose initially (all formulations), then give one-fourth the total loading dose every 6 to 8 hours for two doses (IV and tablets), or give additional fractions every 4 to 8 hours (oral solution). -IV: 8 to 12 mcg/kg -Tablets: 10 to 15 mcg/kg -Oral solution: 10 to 15 mcg/kg.
  • 55. Intro to Atherosclerosis • Atherosclerosis (also known as Arteriosclerotic Vascular Disease or ASVD) the condition in which an artery wall thickens as the result of a build-up of fatty materials such as cholesterol affecting arterial blood vessels, a chronic inflammatory response in the walls of arteries due to the accumulation of macrophage white blood cells and promoted by Low-density lipoproteins without adequate removal of fats and cholesterol from the macrophages by functional high density lipoproteins
  • 56. • It is commonly referred to as a hardening or furring of the arteries. • It is caused by the formation of multiple plaqueswithin the arteries. • It can restrict blood flow. These plaques can also burst, causing a blood clot. • Although atherosclerosis is often considered a heart problem, it can affect arteries anywhere in your body. • Atherosclerosis is a preventable and treatable condition.
  • 57. Causes Atherosclerosis starts with damage or injury to the inner layer of an artery. The damage may be caused by: • High blood pressure • High cholesterol • An irritant, such as nicotine • Certain diseases, such as diabetes
  • 58. Pathophysiology • Atherosclerosis develops as a chronic inflammatory response of the arterial wall to endothelial injury. • Lesion progression occurs through interactions of modified lipoproteins, monocyte-derived macrophages, T-lymphocytes, and the normal cellular constituent of the arterial wall. • The contemporary view of atherosclerosis is expressed by the response-to-injury hypothesis.
  • 59. Response-to-injury hypothesis • The following are the steps involved in the hypothesis: 1. Chronic endothelial injury 2. Accumulation of lipoproteins 3. Monocyte adhesion to the endothelium 4. SMC proliferations and ECM production 5. factor release 6. platelet adhesion
  • 60. 1. Chronic endothelial injury • with resultant endothelial dysfunction, causing increased permeability, leukocyte adhesion, and thrombosis Response-to-injury hypothesis
  • 61. 2. Accumulation of lipoproteins • (mainly LDL and its oxidized forms) in the vessel wall. Low-density lipoprotein molecules (LDL) becoming oxidized (ldl-ox) by free radicals, particularly oxygen free (ROS). When oxidized LDL comes in contact with an artery wall, a series of reactions occur to repair the damage to the artery wall caused by oxidized LDL. Cholesterol can move in the bloodstream only by being transported by lipoproteins Response-to-injury hypothesis
  • 62. 3. Monocyte adhesion to the endothelium • followed by migration into the intima and transformation into macrophages and foam cells. The body's immune system responds to the damage to the artery wall caused by oxidized LDL by sending specialized white blood cells (macrophages and T- lymphocytes) to absorb the oxidized-LDL forming specialized foam cells. Unfortunately, these white blood cells are not able to process the oxidized-LDL, and ultimately grow then rupture, depositing a greater amount of oxidized cholesterol into the artery wall. This triggers more white blood cells, continuing the cycle. Response-to-injury hypothesis
  • 63. 4. platelet adhesion 5. factor release • from activated platelet, macrophages and vascular wall cells, inducing SMC recruitment, either from the media or from the circulating precursors Response-to-injury hypothesis
  • 64. 6. SMC proliferations and ECM production. • Eventually, the artery becomes inflamed. The cholesterol plaque causes the smooth muscle cells to enlarge and form a hard cover over the affected area. This hard cover is what causes a narrowing of the artery, reduces the blood flow and increases blood pressure. Response-to-injury hypothesis
  • 65. 7. Lipid accumulation • both extracellularly and within cells (macrophages and SMC’s). accumulation if lipid-containing macrophages in the intima gives rise to “fatty streaks”, with further evolution, a fibrofatty atheroma consisting of proliferated SMC, foam cells, extracellular lipid, and ECM is formed. Response-to-injury hypothesis
  • 66. Atherosclerosis symptoms depend on which arteries are affected. For example: • Atherosclerosis in heart arteries, have symptoms similar to those of a heart attack, such as chest pain (angina). • Atherosclerosis in the arteries leading to brain, have symptoms such as sudden numbness or weakness in your arms or legs, difficulty speaking or slurred speech, or drooping muscles in your face. • Atherosclerosis in the arteries in arms and legs, produces decreased blood flow is called peripheral artery occlusive disease (PAOD).have symptoms such as leg pain when walking • Sometimes atherosclerosis causes erectile dysfunction in men. Symptoms
  • 67. Depending on the results of the physical exam, doctors may suggest one or more diagnostic tests, including: • Blood tests. • Doppler ultrasound • Ankle-brachial index. • Other imaging tests. • Angiogram. • Electrocardiogram (ECG). Tests and diagnosis
  • 68. Plants used in Atherosclerosis
  • 69. Allium sativum • Common Name:Garlic. Botanical Name:Allium sativum. • Part Used:Bulbs and Rhizome. Family: Amaryllidaceae. Geographical distribution:Garlic is native to Central Asia (Kazakhstan, Kyrgyzstan, Turkmenistan, Tadzhikistan and Uzbekistan) and northeastern Iran • Chemical costituents: Garlic contains 0.1-0.36% of a volatile oil. These are generally considered to be responsible for most of the pharmacological properties of garlic. Garlic contains at least 33 sulfur compounds like aliin, allicin, ajoene, allylpropl, diallyl, trisulfide, sallylcysteine, vinyldithiines, S-allylmercaptocystein, and others. Besides sulfure compounds garlic contains 17 amino acids and their glycosides, arginine and others. Minerals such as selenium and enzymes like allinase, peroxidases, myrosinase etc. the most biologically active compounds, allicin (diallylthiousulfinate or diallyl disulfide) does not exist in garlic until it is crushed or cut; injury to the garlic bulb activates the enzyme allinase, which metabolizes alliin to allicin
  • 70. • Mechanism of Action: • Intact cells of garlic bulbs include an odorless, sulfur-containing amino acid known as allinin. • When garlic is crushed, allinin comes into contact with allinase, which converts allinin to allicin. Allicin has potent antibacterial properties, but it is also highly odoriferous and unstable. • Ajoenes, self-condensation products of allicin, appear to be responsible for garlic's antithrombotic activity. • Fresh garlic releases allicin in the mouth during the chewing process. Dried garlic preparations lack allicin but contain allinin and allinase. Since allinase is inactivated in the stomach, dried garlic preparations should be coated with enteric so that they pass through the stomach into the small intestine where allinin can be enzymatically converted to allicin.
  • 71. • Medicinal Uses: • Lipid-lowering Effects: Garlic's lipid lowering effects may occur via inhibition of HMG-CoA reductase or other enzymes, possibly by diallyl di- and trisulphide components of garlic. • Platelet Effects: Garlic and its derived compound ajoene have demonstrated inhibition of platelet aggregation In vitro and in animals, and reduction of platelet-dependent thrombus formation. • Fibrinolytic Effects: Increased fibrinolytic activity may account for some degree of garlic's anti-clotting effects, involving fibrinogen and plasminogen. • Antimicrobial Effects (Bacteria, Fungi, Yeast): Garlic has been demonstrated In vitro to exert activity against multiple pathogens, including bacteria, including resistant strains, mycobacteria, Helicobacter pylori and fungi. Garlic extract has been found to be bactericidal to Histoplasmacapsulatum.Ajoene alone possesses antibacterial activity against both gram positive and negative bacterial species and inhibits yeast growth In vitro, and the disulfide bond in ajoene may be responsible for these effects. • Lowering of blood glucose and blood pressure; and liver protection. • Unani physicians also use garlic to treat paralysis, forgetfulness, tremor, colic pains, internal ulcers and fevers.
  • 72. • DOSAGE: 1. Atherosclerosis:A 300 mg garlic powder tablet taken as a single dose or three times daily. • 2. For colon cancer and rectal cancer: Capsules containing 2.4 mL of aged garlic extract taken daily for 12 months have been used. • 3. For high blood pressure: 300 mg to 1500 mg of garlic tablets taken in divided doses daily for 24 weeks. • 4. For fungal skin infections (ringworm, jock itch, athlete's foot): garlic ingredient ajoene as a 0.4% cream, 0.6% gel, and 1% gel applied twice daily for one week has been used.
  • 73. Punica granatum • Common Name:Pomegranate. Botanical Name: Punicagranatum Linn • Part Used: Fruit • Family: Lythraceae • Geographical region: Pomegranate is native to a region from Iran to northern India. Pomegranates have been cultivated throughout the Middle East, South Asia, and Mediterranean region for several millennia, and also thrive in the drier climates of California and Arizona • Chemical constituents: • Punicalagin • Punicallin • Punic acid • Gallagicacid • Granatin A • Casuarinin, • Pseudopelletierene
  • 74. • Mechanism of action and medicinal uses: • The potential therapeutic properties of pomegranate are wide-ranging and include treatment and prevention of cancer, cardiovascular disease, diabetes, dental conditions, erectile dysfunction, and protection from ultraviolet (UV) radiation. • Other potential applications include infant brain ischemia, Alzheimer’s disease, male infertility, arthritis, and obesity. Plant pacifies tridosha, tapeworm infestation, • Increase digestive power; alleviate fatigue and thirst and aphrodisiac. • The juice of fresh leaves and young Pomegranate is given in dysentery. • The powdered bark is given for expelling roundworms. • According to Kirtikar and Basu (1935) the unripe fruits and flowers are useful in inducing vomiting, the rind of the fruit is given in diarrhoea and dysentery. • They also strengthen the gums. • Ripe fruit is tonic, laxative and enriches the blood. • The flower-buds are astringent, and are given in chronic diarrhoea and dysentery.
  • 75. • Dose: • As an antioxidant 1000 milligrams of pomegranate extract in the form of POMx™ capsules has been taken by mouth daily for four weeks. A dose of 50 milliliters of pomegranate juice has been taken by mouth daily for three months. • A dose of 100 grams of fresh pomegranate fruit has been taken by mouth for 10 days.
  • 76. REFERENCES • http://jamanetwork.com/journals/jamainternalmedicine/fulla rticle/210378 • http://www.sigmaaldrich.com/life-science/nutrition- research/learning-center/plant-profiler/allium-sativum.html • Bentley and Trimen, Med. Plants 281. 3. Benkeblia, N. 2004. Antimicrobial activity of essential oil extracts of various onions Allium cepa& Garlic (Alliceasatium) lebeusmwiss-uTechnol. 373. • Chemical constituents of cultivated onion Allium cepaLiliaceae. • https://restorativemedicine.org/journal/the-use-of- convallaria-and-crataegus-in-the-treatment-of-cardiac- dysfunction/.

Editor's Notes

  1. About 25% of the world has hypertension or high blood pressure, which basically means 0:10 that someone in your family or circle of friends probably has it - perhaps even you. 0:11 Let’s start with defining it - typically it’s represented by two numbers: the top 0:16 number is the systolic blood pressure which is the arterial pressure when the heart is 0:21 contracting, and the lower number is the diastolic blood pressure which is the arterial pressure 0:25 when the heart is relaxing or refilling. Most of the time blood pressure is taken in the 0:30 brachial artery in your upper arm and if the pressure is high there, then it’s probably 0:34 high throughout all of the arteries. 0:38 Normal blood pressure is between 90 and 119 mmHg systolic, and between 60 and 79 mmHg 0:47 diastolic. Prehypertension, or on the high side of normal, 0:50 is between 120 and 139 mmHg systolic, and between 80 and 89 diastolic. 0:59 Stage 1 hypertension is between 140 and 159 mmHg systolic, and between 90 and 99 diastolic. 1:08 Stage 2 hypertension is between 160 and 179 mmHg systolic, and between 100 and 109 diastolic. 1:18 Stage 3 hypertension is anything over 180 mmHg systolic and 110 mmHg diastolic. 1:27 Typically both systolic and diastolic pressures tend to climb or fall together, but that’s 1:32 not always the case. Sometimes you may have systolic or diastolic hypertension, where 1:36 one number is normal, and the other is really high, and in that situation it’s called 1:40 isolated systolic hypertension or isolated diastolic hypertension. 1:47 Having high pressures is a serious problem for the blood vessels because it causes wear 1:50 and tear on the endothelial cells that line the inside of the blood vessels. Like a garden 1:56 hose that’s always under high pressures, long-term the blood vessels can develop tiny 2:00 cracks and tears that can lead to serious problems such as myocardial infarctions, aneurysms, 2:05 and strokes. 2:07 About 90% of the time, hypertension happens without a clearly identifiable underlying 2:12 reason, and we call this primary hypertension or essential hypertension. In other words, 2:18 over time the pressure in the arteries begins to silently creep up. There are a risk-factors 2:23 that we’ve identified for primary hypertension, these include old-age, obesity, salt-heavy 2:29 diets, and sedentary lifestyles. With the exception of age, all of these can be improved 2:34 with lifestyle changes, and those changes can help reduce hypertension. 2:40 About 10% of the time, there is a specific underlying condition that can be found which 2:45 is the cause of hypertension. For example, anything that limits the blood flow to the 2:52 kidneys can cause hypertension, for example atherosclerosis, vasculitis, or aortic dissections 2:59 affecting renal blood flow. This is because the kidneys play an important role in blood 3:03 pressure regulation. When not enough blood is flowing to the kidneys, the kidney secretes 3:07 the hormone renin which ultimately helps the kidneys retain more water. That water contributes 3:13 to filling the arteries and making them more full which leads to higher pressures. 3:18 Other diseases can cause secondary hypertension as well. Actually quite a few. Fibromuscular 3:22 dysplasia which affects young women can cause the walls of the large- and medium-sized arteries 3:26 to thicken. If it involves the renal artery, and limits blood flowing to the kidneys, it 3:31 triggers more renin. Another one is a tumor that produces excess aldosterone, and like 3:37 renin, excess aldosterone leads to fluid retention. 3:42 Another way to think about hypertension is to categorize it as benign hypertension or 3:45 malignant hypertension. Benign hypertension is any hypertension that is in stage 1 or 3:50 stage 2, and typically it causes no immediate symptoms. Malignant hypertension is really 3:56 severe stage 3 hypertension, and is an emergency because it can cause increased intracranial 4:01 pressure and organ damage.
  2. When there’s extra sodium in your bloodstream, it pulls water into your blood vessels, increasing the total amount (volume) of blood inside your blood vessels. With more blood flowing through your blood vessels, blood pressure increases. It’s like turning up the water supply to a garden hose — the pressure in the hose increases as more water is blasted through it. Over time, high blood pressure may overstretch or injure the blood vessel walls and speed the build-up of gunky plaque that can block blood flow. The added pressure also tires out the heart by forcing it to work harder to pump blood through the body.
  3. Angina comes from the latin angere, which means to strangle, and pectoris comes from 0:09pectus, meaning chest—so angina pectoris loosely translates to “strangling of the 0:15chest”, which actually makes a lot of sense, because angina pectoris is caused by reduced 0:19blood flow which causes ischemia to the heart muscle, or lack of oxygen to the heart, almost 0:24like the heart’s being strangled which causes terrible chest pain. 0:29Stable angina or chronic angina is the most common type of angina and it usually happens 0:33when the patient has greater than or equal to 70% stenosis, meaning 70% of the artery 0:38is blocked by plaque buildup. 0:41This small opening that blood flows through might be enough to supply the heart during 0:44rest, but if the body demands more blood and oxygen, like during exercise or stressful 0:48situations, the heart has to work harder, and therefore needs more blood and oxygen 0:53itself. 0:54It’s during these time of exertion or emotional stress that people with stable angina have 0:59chest pain, since the blood flow isn’t meeting the metabolic demands of the heart muscle, 1:03or myocardium. 1:05But the pain usually goes away with rest. 1:08In the majority of cases, the underlying cause of stable angina is atherosclerosis of one 1:12or more the coronary arteries—arteries supplying blood to the heart muscles. 1:18Other heart conditions that might lead to stable angina are ones that cause a thickened 1:21heart muscle wall, which would require more oxygen. 1:24This increase in muscle size can be due to hypertrophic cardiomyopathy from a genetic 1:28cause, or as a result from the heart having to pump against higher pressures, as is the 1:32case in aortic stenosis, which is a narrowing of the aortic valve, or hypertension. 1:38These larger, thicker heart muscles require more oxygen, and if the patients can’t meet 1:43increasing demands, they feel pain in the form of angina. 1:47Whatever the case, the heart needs blood, and if we look at the heart wall, there’s 1:50three layers—the outermost layer, the epicardium, then the myocardium in the middle, and the 1:55endocardium inside the heart. 1:58The coronary arteries start up in the epicardium, and then dive down and supply all the heart 2:02tissue. 2:03If blood flow’s reduced or the myocardium is thicker, blood has a harder time reaching 2:08this deeper layer just under the endocardium, called the subendocardium. 2:13Therefore the classic finding with angina is subendocardial ischemia, meaning less oxygen 2:17is reaching the region just under the endocardium. 2:21This ischemia is thought to trigger release of adenosine, bradykinin, and other molecules 2:25that stimulate nerve fibers in the myocardium that result in the sensation of pain. 2:31That chest pain is usually described as feeling like pressure or squeezing and it can radiate 2:35to the left arm, jaw, shoulders, and back, and sometimes is accompanied by shortness 2:39of breath and diaphoresis or sweating. 2:43Usually the pain and symptoms last less than 20 minutes and subside after the exertion 2:47or stress is taken away, and therefore the heart muscle isn’t demanding as much blood. 2:51Now, unlike stable angina which describes when patients have pain only during periods 2:56of exertion or stress, but not during rest, there is also unstable angina which is when 3:01patients have pain during exercise or stress as well as during rest—it never really goes 3:05away. 3:07Unstable angina is usually caused by rupture of atherosclerotic plaque with thrombosis, 3:12meaning a blood clot forms on top of a mound of plaque. 3:16Although the occlusion might not block the entire vessel, there is now even less room 3:20left for blood to flow by, and the heart tissue is starting to feel starved for oxygen even 3:23while pumping at a normal rate. 3:26Unstable angina, for the same reason as stable angina, involves subendocardial ischemia and 3:31it should be treated as an emergency, because patients are at a high risk of progressing 3:35to myocardial infarction, or heart attack. 3:38The key distinction is that unstable angina means that the heart tissue is alive but ischemic 3:43or starving for oxygen, whereas myocardial infarction means that the areas of heart tissue 3:47have already begun to necrose or die. 3:51Now a third type of angina is vasospastic angina, also known as prinzmetal angina, and 3:57patients may or may not also have atherosclerosis. 4:00Ischemia, and resulting chest pain is due to coronary artery vasospasms, meaning the 4:05smooth muscles around the arteries constrict extremely tightly and reduce blood flow enough 4:10to cause ischemia. 4:12Episodes of vasospastic angina don’t correlate with exertion and can happen anytime, including 4:18at rest. 4:19The underlying mechanism causing vasospasms isn’t well understood, but likely involves 4:24vasoconstrictors like platelet thromboxane A2. 4:29Unlike both stable and unstable angina, in this case the coronary artery’s constricted 4:34so severely that all layers of the heart wall being supplied are affected, therefore it’s 4:38referred to as transmural ischemia. 4:42Alright, so if we line these three up side-to-side, there’s some important clinical similarities 4:48and differences. 4:49First, it’s super important to remember that in each case, the injury to cardiomyocytes 4:53isn’t permanent, meaning it’s reversible and the cardiomyocytes don’t die (which 4:58is how this differs from myocardial infarction). 5:00On an electrocardiogram, or ECG, both stable and unstable angina show an ST-segment depression 5:07since ischemia’s limited to the subendocardium. 5:10In contrast, vasospastic angina shows ST-segment elevation due to transmural ischemia. 5:18Rest tends to relieve stable angina, whereas unstable angina and vasospastic angina can 5:23occur anytime, including at rest. 5:26In terms of medications, all three can be treated with Nitroglycerin which is a vasodilator 5:31that increases blood vessel diameter to allow more blood flow. 5:34In addition, vasospastic angina also responds to calcium channel blockers.
  4. This small opening that blood flows through might be enough to supply the heart during 0:44rest, but if the body demands more blood and oxygen, like during exercise or stressful 0:48situations, the heart has to work harder, and therefore needs more blood and oxygen 0:53itself. 0:54It’s during these time of exertion or emotional stress that people with stable angina have 0:59chest pain, since the blood flow isn’t meeting the metabolic demands of the heart muscle, 1:03or myocardium. 1:05But the pain usually goes away with rest.
  5. heart wall, there’s 1:50three layers—the outermost layer, the epicardium, then the myocardium in the middle, and the 1:55endocardium inside the heart. 1:58The coronary arteries start up in the epicardium, and then dive down and supply all the heart 2:02tissue. 2:03If blood flow’s reduced or the myocardium is thicker, blood has a harder time reaching 2:08this deeper layer just under the endocardium, called the subendocardium. 2:13Therefore the classic finding with angina is subendocardial ischemia, meaning less oxygen 2:17is reaching the region just under the endocardium. This ischemia is thought to trigger release of adenosine, bradykinin, and other molecules 2:25that stimulate nerve fibers in the myocardium that result in the sensation of pain. 2:31That chest pain is usually described as feeling like pressure or squeezing and it can radiate 2:35to the left arm, jaw, shoulders, and back, and sometimes is accompanied by shortness 2:39of breath and diaphoresis or sweating. 2:43Usually the pain and symptoms last less than 20 minutes
  6. it should be treated as an emergency, because patients are at a high risk of progressing 3:35to myocardial infarction, or heart attack.
  7.  A transmural MI is characterized by ischemic necrosis of the full thickness of the affected muscle segment(s), extending from the endocardium through the myocardium to the epicardium.